ArticleAmerican journal of physiology. Renal physiology2013
Urine concentration in the diabetic mouse requires both urea and water transporters.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Quercetin prevents kidney against diabetes mellitus (type 1) in rats by inhibiting TGF-β/apelin gene expression.Molecular biology reports · 2024Article
- Phosphatases Decrease Water and Urea Permeability in Rat Inner Medullary Collecting Ducts.International journal of molecular sciences · 2023Article
- Purinergic signaling is enhanced in the absence of UT-A1 and UT-A3.Physiological reports · 2021Article
- Inhibition of urea transporter ameliorates uremic cardiomyopathy in chronic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Lack of urea transporters, UT-A1 and UT-A3, increases nitric oxide accumulation to dampen medullary sodium reabsorption through ENaC.American journal of physiology. Renal physiology · 2019Article
- The Expression of AQP5 and UTs in the Sweat Glands of Uremic Patients.BioMed research international · 2017Article
- Effect of Dapagliflozin Treatment on Fluid and Electrolyte Balance in Diabetic Rats.The American journal of the medical sciences · 2016Article
- Transgenic Restoration of Urea Transporter A1 Confers Maximal Urinary Concentration in the Absence of Urea Transporter A3.Journal of the American Society of Nephrology : JASN · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The regulation of the inner medullary collecting duct (IMCD) urea transporters (UT-A1, UT-A3) and aquaporin-2 (AQP2) and their interactions in diabetic animals is unknown. We investigated whether the urine concentrating defect in diabetic animals was a function of AQP2, the UT-As, or both transporters. UT-A1/UT-A3 knockout (UT-A1/A3 KO) mice produce dilute urine. We gave wild-type (WT) and UT-A1/A3 KO mice vasopressin via minipump for 7 days. In WT mice, vasopressin increased urine osmolality from 3,000 to 4,550 mosmol/kgH(2)O. In contrast, urine osmolality was low (800 mosmol/kgH(2)O) in the UT-A1/A3 KOs and remained low following vasopressin. Surprisingly, AQP2 protein abundance increased in UT-A1/A3 KO (114%) and WT (92%) mice. To define the role of UT-A1 and UT-A3 in the diabetic responses, WT and UT-A1/A3 KO mice were injected with streptozotocin (STZ). UT-A1/A3 KO mice showed only 40% survival at 7 days post-STZ injection compared with 70% in WT. AQP2 did not increase in the diabetic UT-A1/A3 KO mice compared with a 133% increase in WT diabetic mice. Biotinylation studies in rat IMCDs showed that membrane accumulation of UT-A1 increased by 68% in response to vasopressin in control rats but was unchanged by vasopressin in diabetic rat IMCDs. We conclude that, even with increased AQP2, UT-A1/UT-A3 is essential to optimal urine concentration. Furthermore, UT-A1 may be maximally membrane associated in diabetic rat inner medulla, making additional stimulation by vasopressin ineffective.
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